Partial Response to Pyrotinib Plus Capecitabine in an Advanced Breast Cancer Patient with HER2 Amplification and R157W Mutation After Anti-HER2 Treatment: A Case Report and Literature Review

Yanchun Qu,1– 3,* Yufeng Liu,3,* Kailin Ding,3 Yong Li,1,2 Xiaoyu Hong,4 Haibo Zhang1,2 1Department of Oncology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China; 2Department of Oncology, Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou, People’s Republic of China; 3The Second Clinical Medical College of Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China; 4Nanjing Geneseeq Technology Inc, Nanjing, People’s Republic of China*These authors contributed equally to this workCorrespondence: Haibo ZhangDepartment of Oncology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, No. 111 Dade Road, Yuexiu District, Guangzhou, 510120, People’s Republic of ChinaTel +86-020-81887233Email haibozh@gzucm.edu.cnAbstract: Human epidermal growth factor receptor2 (HER2) overexpression/amplification is associated with high malignancy, rapid disease progression and poor overall survival in breast cancer. The application of anti-HER2 drugs has greatly improved the survival of patients with HER2-positive breast cancer, but drug resistance issues affect the long-term efficacy. The HER2 mutation is considered to be one of the reasons for resistance to anti-HER2 therapy, and there is currently no standard treatment. We report for the first time the detection of HER2 amplification with R157W mutation by second-generation sequencing (NGS) in a 57-year-old hormone receptor-negative, HER2-positive woman with advanced breast cancer who was resistant to multi-line anti-HER2 therapies. She subsequently received pyrotinib combined with capecitabine treatment and achieved partial response. The small-molecule pan-HER family irreversible inhibitor pyrotinib combined with capecitabine has shown a promising effect in the treatment of HER2 mutation-induced resistance, but the molecular mechanism and efficacy need to be further verified.Keywords: breast cancer, HER2 amplification, HER2 R157W mutation, pyrotinib plus capecitabine, anti-HER2 treatment